Chronic effects of streptozotocin-induced diabetes on the ultrastructure of rat ventricular and papillary muscle

Contractile dysfunctions have been demonstrated in different experimental m odels of diabetes which have similar characteristics to many of the abnorma lities found in the clinical setting. Administration of streptozotocin (STZ ) to young adult rats induces beta -cell necrosis of the pancreas which giv es rise to hypoinsulinaemia and hyperglycaemia, features which are also see n in untreated type 1 clinical diabetes. We have investigated the chronic e ffects of STZ-induced diabetes on contraction in rat ventricular myocytes a nd ultrastructure of cardiac muscle. Diabetes was induced in male Wistar ra ts (230-270 g) with a single injection of STZ (60 mg kg(-1)). At 2 and 10 m onths after STZ treatment, the amplitude of contraction was larger in diabe tic compared to control myocytes. Time to peak contraction was significantl y longer at 2 months but appeared to normalise at 10 months after STZ treat ment. In contrast, time to half relaxation of contraction was not significa ntly different after 2 months but was significantly reduced at 10 months af ter STZ treatment compared to control. Transmission electron microscope exa mination of cardiac muscle showed that the ultrastructure of cardiac muscle , especially structures associated with contraction, were not greatly alter ed after STZ treatment. Sarcomere lengths were not significantly different in papillary or ventricular muscle at 4 or 8 months after STZ treatment com pared to control. Our data provide evidence that morphological defects in c ontractile myofilaments and associated structures cannot explain contractil e dysfunctions seen in ventricular myocytes from STZ-treated animals.